UK Researchers have discovered a gene that helps combat multiple sclerosis (MS). The research, published early online in the journal Nature, found that the gene which puts a person at risk of MS, called DR2b, is partnered by another gene, DR2a, which tempers the effects of the risk gene and reduces the severity of MS symptoms. It is hoped, when more knowledge is gained about this protective gene, that it may be exploited for potential therapies.
MS is a disease that affects around 85,000 people in the UK. It is caused by the immune system attacking the body's own tissue. MS is the result of damage to myelin, a protective sheath surrounding nerve fibres of the central nervous system. When myelin is damaged, messages between the brain and other parts of the body are disrupted. This results in a wide range of symptoms including pain, muscle problems, impaired brain function and impaired vision. The precise cause of MS is currently unclear, but many factors, both environmental and genetic, are understood to be involved. Around two thirds of MS sufferers carry the DR2 pair of genes, although carrying these genes does not necessarily mean an individual will develop MS.
Professor Lars Fugger, one of the lead researchers from the Medical Research Council Human Immunology Unit explains 'The DR2b gene clearly tells the immune system to go hard into battle against the body's own tissue, so it starts to work in a way that actually damages the person. For this reason, natural selection has eliminated the gene on its own, but allowed it to be inherited only when it is accompanied by another gene [DR2a] which tempers its effect.' DR2a redirects the immune system to prevent it attacking the body.
Researchers looked at mice which had been genetically altered to carry different combinations of DR2a and DR2b to observe how the two genes interact to affect severity of MS symptoms. They discovered that mice engineered to carry only the DR2b gene had a severe form of MS that is seen in a minority of MS patients. The mice with both genes however, were less likely to develop MS, but if they did, they had a milder form of the disease that resembles the most common form in humans.
The researchers are hopeful that DR2a's ability to relieve MS symptoms may be exploited for future therapies. The research also provides new hope for other diseases caused by defective functioning of the body's immune system. Professor Fugger said 'This is a new way to assess how genes contribute to autoimmune diseases overall. Thus this study is not only relevant to understand how genes interact in MS, but also in diabetes, rheumatoid arthritis and psoriasis which are all autoimmune diseases'